Obesity and overweight are significant medical and social problems, and current approaches to their treatment, including hypocaloric diets, bariatric interventions, and pharmacotherapy, including incretin drugs (e.g., glucagon-like peptide-1 receptor agonists), can be accompanied by the development of diffuse hair loss. This article, prepared following a discussion at an expert council, systematizes current data on the prevalence and clinical and morphological variants of alopecia associated with weight loss. The main pathogenic mechanisms are discussed, including metabolic stress, protein-energy malnutrition, and micronutrient deficiencies.

Special attention is paid to the role of biotin and vitamin D in maintaining hair follicle function, as well as to risk groups for alopecia in patients undergoing treatment for obesity. Approaches to the prevention, monitoring, and comprehensive management of such patients are presented, taking into account the need to maintain adherence to the main therapy.

This article systematizes current data on the prevalence and clinical and morphological variants of alopecia associated with weight loss. It examines the main pathogenic mechanisms, including metabolic stress, protein-energy malnutrition, and micronutrient deficiencies. Special attention is paid to the role of biotin and vitamin D in maintaining hair follicle function, as well as to risk groups for alopecia in patients undergoing treatment for obesity. Approaches to prevention, monitoring, and comprehensive management of these patients are presented, taking into account the need to maintain adherence to the primary therapy.

On March 25, 2026, a meeting of the Expert Council entitled "Hypoparathyroidism in the Era of Complex Challenges and Breakthrough Technologies" was held in Moscow at the Endocrinology Research Centre. The meeting focused on the epidemiology of chronic hypoparathyroidism (hypoPT) in Russia, the specifics of patient management with this pathology in other countries, and the similarities and differences between international and Russian clinical guidelines.

The meeting discussed advances in improving diagnostics and personalized treatment for patients with hypoPT in Russia, as well as the need to implement best practices in practical healthcare as part of the 2027 clinical guidelines revision.

The importance of including chronic hypoPT in the official list of rare (orphan) diseases was highlighted, as was the need to continue studying the characteristics of the disease and its complications, diagnosis, monitoring, and prevention of hypoPT, including in the long term. The meeting also highlighted the relevance of an interdisciplinary professional alliance to achieve optimal treatment outcomes and improve the quality of life of patients with chronic hypoPT. The experts highlighted the need to implement innovative, effective treatment methods, including hormone replacement therapy for hypoPT. The Council discussed the efficacy and safety of the new therapeutic technology, TransCon parathyroid hormone. Invited expert Dilek Gogas Yavuz, MD, Professor at the Marmara University School of Medicine, Department of Endocrinology and Metabolism, Department of Internal Medicine (Istanbul, Turkey), shared her experience with the drug and the results of international clinical trials. This resolution is a summary of the issues discussed in the Council members’ presentations and during the professional discussions.

BACKGROUND: Although pheochromocytomas and paragangliomas (PPGLs) classically present with distinct clinical signs, there is a category of patients with asymptomatic disease course. Despite the absence of clinical manifestations, these patients retain the risk of life-threatening hypertensive crisis and other cardiovascular complications. The clinical, laboratory, and imaging characteristics of asymptomatic PPGLs remain insufficiently studied and are of significant scientific and practical interest.

AIM: To analyze the clinical, laboratory, and imaging characteristics of asymptomatic PPGLs compared to symptomatic ones.

MATERIALS AND METHODS: The analysis included 347 patients with histologically confirmed PPGL who underwent surgery at the Saint Petersburg State University Hospital. Retrospective analysis encompassed demographic data, medical history (primary and comorbid conditions), laboratory findings, and computed tomography (CT) data. RESULTS: The PPGLs patient cohort included 45 cases without clinical signs of catecholamine hypersecretion. The asymptomatic subgroup, compared to symptomatic patients, exhibited younger age (43 [33; 51] vs. 48 [37; 57] years); smaller maximum tumor size (34 [27; 53] vs. 45 [34; 60] mm); lower metanephrine/normetanephrine ratio (0.29 [0.10; 0.79] vs. 0.51 [0.09; 1.23]).

CT imaging revealed slightly higher radiodensity values in asymptomatic PPGLs during arterial, venous, and delayed phases compared to symptomatic tumors. However, absolute and relative washout percentages did not differ significantly.

CONCLUSION: The younger age and smaller tumor size in asymptomatic PPGL patients suggest earlier detection of the disease compared to symptomatic cases. The lower metanephrine/normetanephrine ratio may indicate a higher prevalence of the norepinephrine-secreting phenotype in asymptomatic PPGLs. No pronounced differences were found in imaging characteristics between asymptomatic and symptomatic tumors.

BACKGROUND: A combination of endogenous hypercortisolism and primary hyperparathyroidism (PHPT) occurs rarely, few clinical cases are described in the literature. The causes of the development of such combination are poorly investigated. AIM: To study clinical and genetic characteristics of a combination of endogenous hypercortisolism and PHPT.

MATERIALS AND METHODS: A retrospective, single-center, cross-sectional, observational study was performed. Clinical characteristics of patients with a combination of endogenous hypercortisolism and PHPT were analyzed. All patients had previously undergone genetic testing as follows: MEN1 Sanger sequencing (n=10), next-generation sequencing of a panel of genes including MEN1 and CDKN1B (n=3), whole-exome sequencing (n=8).

RESULTS: 21 patients (17 females, 4 males) were included in the study: 17 with Cushing’s disease (CD) and PHPT, 3 patients with Cushing’s syndrome (CS) and PHPT, and one patient with ACTH-ectopic syndrome (ACTH-ES) and PHPT. Among patients with CD and PHPT ten had MEN1 mutations (multiple endocrine neoplasia type 1 syndrome (MEN1)), and seven did not have MEN1 mutations (MEN1 phenocopies). In patients with MEN1 the debut of both CD and PHPT occurred at younger age in comparison to MEN1 phenocopies (p=0,015 and p=0,0006). In 60% of MEN1 CD occured in infancy, and in all children CD was the first manifestation. In 75% of adult MEN1 patients CD was diagnosed after PHPT, whereas in all MEN1 phenocopies PHPT was diagnosed after or during investigation with regard to CD. The majority of MEN1 patients also had gastro-entero- pancreatic neuroendocrine tumors (NETs), and some had lung NETs, whereas patients with MEN1 phenocopies did not have NETs. One patient with CS (bilateral lesions) and PHPT had ARMC5 mutation. In a patient with ACTH-ES and PHPT no mutations were found.

CONCLUSION: A combination of endogenous hypercortisolism and PHPT occurs more frequently in females. In children with MEN1 and in MEN1 phenocopies the first manifestation is more frequently CD, while PHPT is diagnosed accidentally during evaluation, whereas in adults with MEN1 the first manifestation is more frequently PHPT. MEN1 mutations can be the cause of a combination of these two endocrine tumor diseases, and, possibly, ARMC5 mutations in cases of CS and PHPT, though in the majority of cases the cause remains unknown. Identification of causes of endogenous hypercortisolism and PHPT co-occurrence can expand our understanding of the mechanisms of endocrine tumor development.

Vitiligo is a dermatological disease characterized by focal disappearance of the melanin pigment on the skin and mucous membranes of a person. Despite the variety of proposed hypotheses for the development of this pathology, the central role belongs to the autoimmune mechanism of melanocyte damage.

Analysis of the results of numerous international studies confirms a pronounced tendency towards an increase in the prevalence of endocrine autoimmune diseases among patients with vitiligo compared to the general population. Such diseases include, first of all, autoimmune thyroiditis, Graves' disease, type I diabetes mellitus and autoimmune adrenal insufficiency. Some studies confirm a high frequency of vitiligo combination with multiendocrine autoimmune syndromes.

This review is aimed at systematizing the available scientific literature on the frequency of occurrence and characteristics of associated autoimmune endocrine disorders in individuals suffering from vitiligo.

Thyrotoxic crisis (TC) is a rare but potentially life-threatening complication of decompensated thyrotoxicosis that requires immediate medical intervention. The diagnosis of TC is based on a clinical picture of severe hyperthyroidism in combination with precipitating factors. Treatment should be initiated at the first suspicion of crisis development, without waiting for the results of hormonal analysis, which may take considerable time to obtain. This article presents a clinical case of a female patient with coexisting Graves’ disease and type 1 diabetes mellitus, in whom TC was promptly recognized and effectively managed. The precipitating factor was diabetic ketoacidosis. This case highlights the importance of early diagnosis and intensive therapy to improve the prognosis of patients with TC.

This article provides a conceptual overview of the methodology and design of prognostic research. It presents cohort studies as the most suitable design for prognostic investigations and discusses in detail the distinctions between traditional etio logical cohort studies and those primarily aimed at predicting outcomes. The article reviews examples of prognostic studies that focus on predicting gestational diabetes mellitus, renal failure in type 2 diabetes mellitus, osteoporotic fractures in postmenopausal women, outcomes of infertility treatment in women with elevated follicle-stimulating hormone levels, and survival in patients with adrenocortical carcinoma. The importance of adhering to the methodological standards outlined in the STROBE and TRIPOD guidelines is emphasized. It also highlights the need to avoid common design and analytical pitfalls, such as measuring predictors after the outcome has occurred or using ROC analysis without developing a multivari able prediction model. Particular attention is given to employing appropriate statistical methods, as a lack of understanding of these methods may lead to biased inferences and diminish the scientific value of the published research. Incorporating well-designed prognostic cohort studies and rigorous analytical approaches will enhance clinical practice and strengthen the evidence base in modern endocrinology.

BACKGROUND: The use of glucocorticosteroids (GCS) in high doses can lead to hyperglycemia. GCS pulse therapy (PT) cause fewer side effects compared to long-term oral administration of GCS in adult patients. Glycemic control in children while GCS PT is not well studied.

AIM: To study short- and long-term effects of methylprednisolone pulse therapy on carbohydrate metabolism parameters in children with autoimmune and autoinflammatory diseases

MATERIALS AND METHODS: We analyzed carbohydrate metabolism parameters of patients before, during, and after PT with methylprednisolone (3 infusions; 0 h, 24 h, 48 h; total dose 27.0 (23.0; 31.6) mg/kg). Observation lasted for 0.2–6.3 years.

RESULTS: We analyzed data from 15 patients (13 girls, 2 boys). During PT, the glycemia level exceeded normal rages in all patients in 4-10 hours after the start of PT, reaching a peak in 7 h – 10.8 (9.9; 11.8) mmol/l. Glycemia peaks 7 h after the second and the third infusions were significantly lower compared to the first day – 9.1 (8.2; 10.7) mmol/l (p<0.05) and 8.9 (7.4; 9.2) mmol/l (p<0.01), correspondently. A tendency toward normalization of glycemia was noted in 24 h after each administration of GCS. Glycemic values in 72 h did not correlate with age, SDS BMI, methylprednisolone dose, and peak glycemic values during PT. There were no significant differences between the glycemic indices of patients undergoing PT for the first time and those who already had experience of PT. Observation for 2.7 (0.5; 4.6) years did not reveal any delayed complications.

CONCLUSION: GCS PT in children resulted in short-term GCS-induced hyperglycemia. Peak glycemia values were observed in 7 hours after each GCS infusion; the rises of glycemia after repeated infusions were lower than after the first one. Spontaneous glycemia normalization was observed in 24 hours after methylprednisolone administration. We did not reveal any delayed disorders of carbohydrate metabolism.

Normophosphatemic familial tumoral calcinosis (NFTC) is characterized by cutaneous calcifications with no metabolic disorders; it manifests in the first years of life; associated with mutations in SAMD9 gene. Chronic trauma and transient hyperphosphatemia play a leading role in calcification formation.

Surgical treatment can remove calcifications, but it does not prevent recurrence and can cause complications. Various conservative therapy is used. Lowering of blood phosphate levels is considered a promising pathogenetic treatment method.

We present a clinical case of a patient with NFTC associated with the homozygous variant p.E1200K in SAMD9. A characteristic feature of our patient is the presence of multiple calcifications not only in the areas of injury (limbs), but also in areas of acne (face), as well as particularly active progression of the disease during puberty. A reduction in calcification size was observed after one year of continuous hypophosphatemic therapy (aluminum hydroxide and sevelamer 800 mg). The effectiveness of this therapy is debatable and limited by both poor patient tolerability of sevelamer and poor adherence.

This is the first description of a patient with molecularly confirmed NFTC in Russia. A precise diagnosis allowed us to clarify the pathogenetic mechanism of calcification formation and propose treatment options.

Congenital hyperinsulinism (CHI) is a rare, genetically heterogeneous disorder characterized by inappropriate hypersecre tion of insulin by pancreatic beta cells and is the most common cause of persistent hypoglycemia in young children. The in cidence of CHI in the general population ranges from 1:30,000 to 1:50,000 live births. Timely diagnosis and treatment of CHI are critical, as persistent hypoglycemia can lead to irreversible damage to the central nervous system. This review summa rizes current understanding of the etiology and pathogenesis of CHI and presents an up-to-date classification of CHI based on duration, etiology, histological form, and response to diazoxide therapy. A detailed diagnostic algorithm is provided, including provocative tests, molecular genetic testing, and imaging studies. The stages of conservative treatment and indi cations for surgical treatment are discussed. The review is based on updated clinical guidelines and is intended for practicing physicians — pediatricians, endocrinologists, and neonatologists — who care for children with hypoglycemic conditions.

Growth hormone (GH) and insulin-like growth factor-1 (IGF-1) are pivotal hormones regulating not only postnatal growth, development, aging, and longevity but also female reproductive function. In clinical practice, GH is widely utilized as an ad juvant therapy to enhance various clinical outcomes in assisted reproductive technology (ART). It is aimed at increasing the yield and quality of oocytes and embryos, as well as improving pregnancy and live birth rates both in the general population and among patients with GH deficiency. Over the past three decades, the roles of GH and IGF-1 in regulating female repro duction have garnered increasing attention, becoming a major focus of research in both endocrinology and reproductive medicine.

Ageing is multifactorial, genetically and epigenetically programmed biological process. Nowadays ageing is acknowledged as extremely actual scientifical, social and demographical problem. Despite the evidence of interactions between ageing and accumulation of endocrine disruptions, the last 150 years of variegated searches for potential endocrine “elixir of lon gevity” brought contradictive, mutually exclusive and even discouraging results. Fortunately, the discovery of referent lab oratory intervals of hormonal blood levels among elderly people improved the overall situation. Traditional treatment of endocrine hormonal deficiency with replacement therapy does not lead to rejuvenation but to potential damage. That’s why it is more accepted to interpret hormonal changes among elderly people not only as aging but specific adaptation for “successful ageing”. The present review contains modern datas about endocrine ageing of thyroid gland, adrenal glands (hy percorticism, adrenopause), pituitary gland (somatopause, hypoprolactinemia), male (andropause) and female (menopause, hyperandrogenism) hypogonadism.